This invention relates to demand-type pacing systems and methods and, more particularly, to rate-adaptive pacing systems and methods for controlling cardiac pacing rate as a function of a monitored cardiac parameter such as myocardial viability.
Rate adaptive pacemaker systems are known in the art and are receiving increasing attention and commercialization. Historically, the first rate adaptive pacing systems have been the dual chamber systems, e.g. atrial synchronous systems, where the pacing of the ventricle is coupled to or synchronized with detected atrial beats. Such dual chamber systems have the clear advantage of optimally simulating normal physiological response, since they derive the timing of the pacing pulses from the atrial response which is induced by the natural heart pacemaker. However, dual chamber systems have certain disadvantages which have been recognized in the literature, as well as certain practical disadvantages. It has been reported that atrial synchronous pacing is not suitable for up to 76% of pacemaker-indicated patients. See Rate Responsive Pacing, Rickards et al, Clin. Prog. Pacing and Electrophysiology, Vol. 1, No. 1, 1983, pp. 12-18.
Dual chamber pacemakers have never been prescribed with the frequency of single chamber pacemakers, for the practical reasons of expense, the need to place pacing leads into both chambers and the potential complexities of dual chamber pacing (such as pacemaker mediated tachycardia) which can be avoided in patients who can be well treated with the simpler single chamber systems.
The single chamber demand pacemaker, while simplest and most reliable in terms of system complexity, carries the fundamental limitation of not being able to adapt its response to normal patient needs. It is well known that the requirements of blood flow vary widely as a function of both physiological (exercise) and emotional occurrences. The normal heart adjusts blood flow by varying both stroke volume and rate, the blood flow being the result of the product of those two variables. While a single chamber pacemaker cannot adjust stroke volume, it can adjust heart rate by the relatively simple technical expedient of adjusting the rate of the delivered pulses. The adjustment of rate alone is considered to provide about 80% of the total blood flow change. See the above-cited Rickards et al paper.
In response to the recognized desirability of being able to automatically adapt pacing rate, e.g., increase exercise tolerance, there has been a great deal of work and progress, including several commercial pacemakers incorporating different feedback systems for controlling pacing rate as a function of one or more sensed cardiac or body parameters. For a summary of such systems, see "Principles of Exercise-Responsive Pacemakers," IEEE Engineering in Medicine and Biology Magazine, Jun. 1984, pp. 25-29; "The Exercise-Responsive Cardiac Pacemaker," IEEE Transaction on Biomedical Engineering, Vol. BME 31, No. 12, Dec. 1984.
The system and method of this invention are based upon our observation that the rate adaptive pacemaker principle is efficiently carried out by controlling the function of one or more parameters which normally and directly control (or are concomitant with) pacing rate in a healthy person. This approach is contrasted to many of the systems that are presently being investigated, wherein indirect parameters such as respiration rate, oxygen saturation, etc. are monitored and utilized in the rate adaptive feedback loop. It is known that there are a number of pathways that directly affect the heart, one being the cardiac sympathetic nerves, and the other being direct release of hormones or catecholamines into the bloodstream. In a normal state the neuroendocrine system stimulates various cardiovascular receptor sites, thus controlling both the heart rate, which is triggered by the natural pacemaker (sinus node) and myocardial contractility which brings about an increase in hemodynamics (pressure-flow). In patients who do not have an intact conduction system, e.g., sino-atrial node dysfunction, the concomitant events that should take place, namely increase in rate and contractility, are disrupted or impaired. Thus we make our observation that the ability to directly detect changes in sympathetic drive, ventricular contractility or circulation catecholamine levels constitute an appropriate means of obtaining information for control of a pacemaker.
It is very unlikely that an artificial chemoreceptor for detecting sympathetic tone or catecholamine level can be perfected in the near future, although such an accomplishment could provide a medically attractively solution to pacemaker control. Another more practical approach for the present in achieving a closed-loop physiologically responsive pacing system is to measure changes in the contractile state of the cardiac muscle itself. This can be accomplished, at least presently, by two different means. A first means is to measure stress in the muscle wall (intramyocardial pressure, or IMP) and the other is to measure the regional wall thickening or fiber-shortening of the muscle. The former can be done by use of ultrasonic A-scan imaging, and the latter with sonomicrometers which are implantable ultrasonic crystals used to measure changes in the relative motion of a given myocardial region. The more feasible approach in terms of practical implementation is the measurement of intramyocardial stress or pressure. The preferred embodiments of our invention, as set forth herein below, utilize the IMP approach.